A mutant protein that plays key role in pancreatic cancer development and growth has been identified by researchers.
The finding from the University of Michigan Comprehensive Cancer Center suggests a possible target for developing new ways to treat this deadly disease.
When Kras is turned off, early stage precancerous pancreatic lesions transform into normal pancreas cells.
Researchers have known that mutations in the Kras gene are what cause pancreatic cancer to develop. These mutations are frequently seen in common precancerous lesions, suggesting it has an early role in pancreatic cancer.
The new study found that in mice, mutant Kras also keeps the tumor growing and helps precancerous tumors grow into invasive cancer. When the researchers turned off Kras, the tumors disappeared and showed no signs of recurring.
The researchers were able to manipulate Kras in a mouse model that they designed to look at Kras at various points in pancreatic cancer development. In the precancerous lesions, turning off Kras eliminated the tumors in mice and the pancreas tissue returned to normal, with no signs of the cancer returning.
With invasive cancer, inactivating Kras killed off the cancer but left the pancreas with fibrous areas similar to scar tissue. Tumors did not recur.
Researchers hope this finding provides the basis for future drug development.
"Right now no drugs specifically target Kras, but there are drugs that target the cellular processes downstream of Kras. We next need to figure out which of these downstream effectors of Kras are important in pancreatic cancer," says study author Marina Pasca di Magliano, Ph.D., assistant professor of surgery and of cell and developmental biology at the U-M Medical School.
The study has been published in the February Journal of Clinical Investigation.